Akademik Veri Yönetim Sistemi
Ankara Universitesi Veteriner Fakultesi Dergisi, cilt.73, sa.2, ss.185-193, 2026 (SCI-Expanded, Scopus, TRDizin)
Valproic acid (2-propyl valeric acid, VPA) is the drug of choice for the treatment of migraine, bipolar disorder, and epileptic disorders in both children and adults. Although VPA has beneficial effects, long-term administration is reported to damage many tissues and organs. VPA administration increases free-radical production. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one, EDA) is a potent antioxidant that protects against oxidative stress. The aim of our study was to investigate the protective effects of EDA against brain damage in VPA-treated rats. Male Sprague Dawley rats were used in our study. The rats were randomly divided into four groups: control, EDA, VPA, and VPA+EDA. EDA and VPA were administered intraperitoneally at doses of 30 mg/kg and 0.5 g/kg, respectively daily for 7 days. On day 8, all animals were sacrificed under anesthesia, and brain tissues were removed. VPA caused decreases in the levels of reduced glutathione (GSH, P<0.05), glutathione peroxidase (GPx, P<0.001), glutathione reductase (GR, P<0.001), and paraoxonase (PON, P<0.0001). On the other hand, VPA increased values of lipid peroxidation (LPO, P<0.05), catalase (CAT, P<0.05), superoxide dismutase (SOD, P<0.0001), glutathione-S-transferase (GST, P<0.01), xanthine oxidase (XO, P<0.01), adenosine deaminase (ADA, P<0.001), protein carbonyl (PC, P<0.0001), myeloperoxidase (MPO, P<0.0001), sialic acid (SA, P<0.0001), and acetylcholinesterase (AChE, P<0.0001) compared with the control group. EDA reversed all values. These results suggest that EDA administration potentially reduces VPA-induced brain injury.